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Fig. 6 Generation of new oligodendrocytes after SCI. (A) Immunostaining for Claudin K (magenta; labelling oligodendrocytes and myelin sheaths) and Neurofilament (grey; labelling axonal filaments) in Tg(olig2:eGFP) sham and 7 dpl fish. In sham controls, OPCs are small and round (sham control, yellow arrowheads) and myelin sheaths enwrap axons in a highly organized manner. SCI results in marked axonal loss and in OPCs becoming reactive (7 dpl, yellow arrowheads). At the same time-point, a proportion of reactive OPCs which is in contact with axons are Claudin K+, indicative of their differentiation into myelinating oligodendrocytes. Images are maximum intensity projections of transverse sections. Scale bars: 10 µm. (B) Timeline of EdU labelling experiment to monitor newly generated oligodendrocytes. (C) SCI causes an increase of newly generated cells (insets, white arrowheads) 700 µm around the lesion site from 5 to 14 dpl. Newly generated oligodendrocytes (mbp:eGFP+/EdU+) can be detected in all areas of the lesioned spinal cord (overview/insets, yellow arrowheads). Images shown are maximum intensity projections of transverse sections. D, dorsal; V, ventral. In the overview images, a white asterisk indicates the central canal. Scale bars: 100 µm. (D) Stereological quantification of mbp:eGFP+/EdU+ cells 700 µm around the lesion site shows a significant increase in the number of newly generated oligodendrocytes at 14 dpl compared to sham controls. Data are mean±s.e.m. Numbers in the plots indicate the number of experimental animals. **P≤0.01 (Mann–Whitney test). Significance is shown compared to sham control. (E) Schematic representation of OPC myelination at 7 dpl and generation of oligodendrocytes by 14 dpl. A proportion of reactive OPCs becomes pre-myelinating, providing fast myelination of spared axons.